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50 Cards in this Set

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What is the general cause of ischemic heart disease (IHD) / coronary artery disease (CAD)?
Reduced blood flow to the myocardium because of:
- Obstructive atherosclerotic lesions in coronary arteries
What are the clinical presentations of ischemic heart disease (IHD) / coronary artery disease (CAD)?
Angina pectoris

Myocardial infarction

Chronic ischemic heart failure

Sudden cardiac death
What are the risk factors for myocardial infarction?
Same risk factors for atherosclerosis

Non-modifiable:
- Age (increases)
- Gender (males, females post-menopause)
- Genetics

Modifiable:
- Hyperlipidemia
- Smoking
- Diabetes
- Hypertension
What are the requisite levels of occlusion in coronary arteries to experience:
- Angina upon exertion
- Angina at rest
Angina upon exertion: 75%

Angina at rest: 90%
What is the first step of the pathogenesis of myocardial infarction?
Sudden change in coronary atheromatous plaque:
- Hemorrhage
- Erosion
- Ulceration
- Rupture
What affect does a sudden change in a coronary atheromatous plaque have on the vessel and what does this trigger?
Endothelial damage

Triggers the hemostatic response
What are the steps of the hemostatic response as caused by endothelial damage in a coronary vessel?
1. Vessel constriction

2. Primary hemostasis:
- Platelet adhesion
- Granule release
- Aggregation

3. Secondary hemostasis with coagulation cascade

4. Thrombus formation
How does the formation of a thrombus on top of a ruptured atheromatous plaque affect blood flow through the coronary artery?
Arterial occlusion
What happens to the myocardium when there is arterial occlusion of a coronary artery?
Myocardial ischemia of the "area at risk" (area supplied by this coronary artery)
What are the changes to myocyte cellular metabolism that are seen with myocardial ischemia?
1. Oxidative phosphrylation stops:
- Decrease in ATP

2. Na+/K+ pump fails:
- Na+ stays inside cell
- Cell swells by taking in H20

3. Anerobic glycolysis begins:
- Increase in lactic acid
- Decrease in pH
- Enzymatic reactions stop
How are myocardial myocytes affected by myocardial ischemia at:
- Seconds after event
- 1 minute after event
- 10 minutes after event
- 30 minutes after event
- 40 minutes after event
Seconds: ATP depletion

1 minute: Loss of contractility

10 minutes: ATP at 50% of normal level

30 minutes: Irreversible damage

40 minutes: ATP at 10% of normal level
At what point does O2 administration during myocardial ischemia result in myocardial infarction as opposed to angina pectoris?
Before 30 minutes: Angina pectoris

After 30 minutes: Myocardial infarction
What are the steps seen following irreversible cell injury and what does this cause?
1. Ca2+ pump failure:
- Myocardial swelling and damage

2. Intracellular enzymes and proteins leak into blood stream:
- Troponin
- CKMB

3. Coagulative necrosis
How does coagulative necrosis appear histologically?
As "contraction band necrosis"
- Myocardial fibers lose cross-striations
- No nuclei
- Dark pink wavy bands across fibers

*EARLIEST CHANGE SEEN IN THE FIRST DAY
What are the events that occur after coagulative necrosis of myocardial myocytes and how do these events appear histologically?
1. Acute inflammation:
- Increased blood flow (congestion and hemorrhage)
- Leaking of plasma proteins (edema)
- Leukocyte recruitment and activation

2. Phagocytosis of dead cells (myocytes and leukocytes) by macrophages

3. Healing via fibrosis
What is the wavefront phenomenon of myocardial infarction?
Necrosis begins in a small zone of the myocardium:
- Beneath endocardial surface
- Center of ischemic zone

Wave front of cell death seen progressing as ischemia persists:
- Through more thickness
- More breadth
Why is the first region of necrosis during a myocardial infarction beneath the endocardial surface?
This region is farthest away from the epicardial vessel
- First to die after blockage
How does the region of myocardium directly beneath the endocardial surface normally obtain enough O2 if it is the farthest away from epicardial coronary vessels?
O2 perfusion from blood in the ventricular lumen
What are the progressive steps of the pathogenesis of myocardial infarction?
1. Sudden change in coronary atheromatous plaque

2. Hemostasis with thrombus formation

3. Arterial occlusion

4. Myocardial ischemia

5. Coagulative necrosis

6. Acute inflammatory response

7. Phagocytosis and healing via fibrosis and scar formation
What are the two types of myocardial infarction?
Subendocardial infarction

Transmural infarction
How extensive is necrosis regarding the ventricular wall in both subendocardial infarction and transmural infarction?
Subendocardial infarction:
- Limited to 1/3 - 1/2 of ventricular wall thickness

Transmural infarction:
- Complete or almost complete necrosis of ventricular wall thickness
How does the level of coronary artery stenosis differ between subendocardial infarction and transmural infarction?
Subendocardial infarction:
- Incomplete occlusion of coronary vessel

Transmural infarction:
- Complete occlusion of coronary vessel
How is the ST segment during an ECG represented during a subendocardial infarrction as opposed to a transmural infarction?
Subendocardial infarction:
- "Non-STEMI": No ST elevation

Transmural infarction
- "STEMI": ST elevation
How old is myocardial infarction based on gross pathological features of this specimen and why?
Recent (days old)
- Dark red hyperemic area
- Due to congestion and hemorrhage
How old is myocardial infarction based on gross pathological features of this specimen and why?
Intermediate (weeks old)
- Yellow / tan and soft
- Red border
- From complete necrosis and phagocytosis
- Healing begins from center
How old is myocardial infarction based on gross pathological features of this specimen and why?
Remote (> 2 months old)
- Grey / white
- Firm scar
- Represents fibrosis
When is the earliest time after a myocardial infarction that gross pathological features are able to be seen?
12 hours
When is the earliest time after a myocardial infarction that microscopic pathological features are able to be seen?
4 hours
How old is myocardial infarction based on microscopic pathological features of this specimen and why?
Recent (days old)
- Edema
- Hemorrhage
- Coagulative necrosis
- Contraction bands
- Neutrophilic infiltrate
How old is myocardial infarction based on microscopic pathological features of this specimen and why?
Intermediate (weeks old)
- Macrophages phagocytosing myocytes and leukocytes
- Granulation tissue beginning to form
How old is myocardial infarction based on microscopic pathological features of this specimen and why?
Remote (> 2 months old)
- Dense collagenous scar
What are the complications associated with myocardial infarction?
Ischemia-reperfusion injury

Myocardial rupture

Pericarditis

Ventricular aneurysm

Infarct extension

Infarct expansion

Cardiogenic shock

Arrythmia
How do myocyte viability and function change with permanent occlusion of a coronary artery as opposed to a temporary occlusion followed by reperfusion and what is a consequence of this?
Consequence:
- Ischemia reperfusion injury
What are the main causes of ischemia reperfusion injury following a myocardial infarction?
Oxygen-derived free radical damage

Inflammation

Complement activation
From where do oxygen-derived free radicals come and how do they damage cardiac myocytes during ischemia reperfusion injury?
Come from mitochondrial respiration and energy generation

Cause oxidative stress when they cannot be eliminated (as in post MI)

Also created by leukocytes as mediators to destroy dead cells
How does complement activation play a role in ischemia reperfusion injury?
IgM deposits on ischemic tissue

With restored blood flow, anti-IgM antibodies bind to these tissues and cause damage
What changes to the myocardium can cause myocardial rupture after a myocardial infarction?
Weakening and softening of the inflamed and necrotic myocardium
What type of myocardial infarction is required to have occurred for there to be a chance of myocardial rupture?
Transmural myocardial infarction
What are the common sites of myocardial rupture after a myocardial infarction?
Free wall (left ventricle)

Papillary muscle (rare)

Ventricular septum (rare)
How long after a myocardial infarction does a myocardial rupture normally occur, if it occurs?
~5 days (10% of cases)

~ Within two weeks (90% of cases)
What are risk factors for myocardial rupture post myocardial infarction?
Increased age

Female

Hypertension

First myocardial infarction

Poor coronary collateral vessels
When, usually, does pericarditis occur post-myocardial infarction?
24-96 hours post-myocardial infarction
What is Dressler's syndrome and what are the symptoms of this condition?
Late pericarditis (1-8 weeks post-myocardial infarction)
- Fever
- Pleuritic pain
- Pericardial effusion

"Post myocardial infarction syndrome)
What type of myocardial infarction usually causes a ventricular aneurysm, if it is caused?
Transmural myocardial infarction
How is the myocardium affected by a ventricular aneurysm?
Bulging of thin myocardial wall during systole
What are the potential consequences of a ventricular aneurysm?
Mural thrombi

Arrythmia

Heart failure
What is infarct extension post-myocardial infarction?
Progressive increase in amount of myocardial necrosis within infarct zone of original myocardial infarction
What causes infarct extension post-myocardial infarction?
Re-occlusion of infarct-related artery after blood flow to infarcted area is restored
How can infarct extension post-myocardial infarction present?
Necrotic and healing myocardium of different ages in the same area
How is the myocardium affected during cases of infarct expansion post-myocardial infarction?
Acute regional dilation and thinning (stretching) of infarcted zone